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Blood, Vol. 94 No. 2 (July 15), 1999:
pp. 684-693
Acute Systemic Reaction and Lung Alterations Induced by an Antiplatelet
Integrin gpIIb/IIIa Antibody in Mice
Bernhard Nieswandt,
Bernd Echtenacher,
Frank-Peter Wachs,
Josef Schröder,
J. Engelbert Gessner,
Reinhold E. Schmidt,
Georges
E. Grau, and
Daniela N. Männel
From the Department of Pathology, Tumor Immunology, University of
Regensburg, Regensburg, Germany; and the Department of Clinical
Immunology, Hannover Medical School, Hannover, Germany.
Shock is frequently accompanied by thrombocytopenia. To investigate
the pathogenic role of platelets in shock, we examined the in vivo
effects of monoclonal antibodies (MoAbs) against mouse platelet
membrane proteins. Injection of the platelet-specific MoAb MWReg30 to
the fibrinogen receptor (gpIIb/IIIa) rendered mice severely hypothermic
within minutes. Isotype-matched control antibodies, even if they also
recognized platelet surface antigens, did not induce comparable signs.
MWReg30 induced early signs of acute lung injury with increased
cellularity in the lung interstitium and rapid engorgement of alveolar
septal vessels. Despite this in vivo activity, MWReg30 inhibited rather
than stimulated platelet aggregation in vitro. MWReg30-binding to
platelets led to phosphorylation of gpIIIa, but did not induce
morphological signs of platelet activation. The MWReg30-induced
reaction was abolished after treatment with MoAbs 2.4G2 to Fc RII/III
and was absent in FcRIII-deficient mice, clearly demonstrating the
requirement for FcRIII on involved leukocytes. Simultaneous
administration of tumor necrosis factor exacerbated, whereas a
tolerizing regimen of tumor necrosis factor or bacterial
lipopolysaccharide completely prevented the reaction. These data
suggest that platelet surface-deposited MWReg30-immune complexes lead
to an acute Fc-mediated reaction with pulmonary congestion and
life-threatening potential that could serve as an in vivo model of
acute lung injury.
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